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Anti-Smooth-Muscle Antibody 

  • Author: Joshua Sloan, DO; Chief Editor: Eric B Staros, MD  more...
 
Updated: Mar 04, 2014
 

Reference Range

Normal: Negative titer[1, 2]

Positive: 1:40[1, 2]

Strongly positive: ≥1:80[1, 2]

There are no differences in race or sex with regard to titer results. Titers may be lower in children and still indicate a positive test for autoimmune hepatitis type 1 (AIH-1).[1]

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Interpretation

Negative titers for anti–smooth-muscle antibody (ASMA) are expected in healthy individuals. Positive titers indicate the presence of several underlying conditions, including the following:

The degree of positivity evidenced by the titer can be used to determine the etiology. Such an approach is especially useful for correlating ASMA positivity with the presence of autoimmune hepatitis, specifically type 1.[3]

In 1999, Alvarez et al developed a scoring system for autoimmune hepatitis type 1 (AIH-1) in which a negative titer yielded 0 points, a titer of 1:40 was 1 point, a titer of 1:80 was 2 points, and a titer of ≥1:80 was 3 points.[1] A definitive diagnosis was determined by a score of >15, while a score of 10-15 indicated a probable diagnosis of AIH-1.[1, 2]

In 2008, Czaja created a scoring system that was simplified from the previous version and proposed that ≥1:40 was 1 point and ≥1:80 was 2 points.[2] In the new scoring system, a definitive diagnosis is ≥7 and a probable diagnosis is 6.[2]

A positive result can also be found in patients with chronic hepatitis B or C.[1, 4, 5] In such individuals, positive hepatitis serologies indicate viral hepatitis as the etiology. Additionally, ASMA can be positive in primary biliary cirrhosis, primary sclerosing cholangitis, and overlap syndromes associated with AIH-1.[1, 3]

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Collection and Panels

Specimen: Blood or serum

Collection method: Routine venipuncture; no patient preparation needed prior collection

Container: Red-Top Vacutainer (no additives)

Storage: Refrigerate at 2-8°C; specimens stable at 1-2 weeks

Panels: Anti–smooth-muscle antibody is part of the autoimmune liver disease panel

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Background

Description

Smooth-muscle antibodies were first discovered in 1965 by Johnson et al when they demonstrated that antibodies in the sera of patients with chronic liver disease were able to bind to the smooth muscle of rat stomachs.[6] These antibodies were later demonstrated to be present in other conditions, including viral hepatitis, malignancy, heroin use, and other autoimmune liver diseases such as primary biliary cirrhosis.[6, 7, 8] As such, the specificity of these antibodies to smooth muscle was questioned, especially when they were shown to also react to striated muscle and renal, thymic, and glomerular cells.[9]

In 1973, Gabbiani et al suggested that smooth-muscle antibodies were probably towards actin when they demonstrated elimination of all smooth-muscle antibody activity in the sera of 5 patients with chronic active hepatitis using a preparation of platelet-derived actin called thrombosthenin A.[10] These findings gave reason for the broad range of tissue reactivity of smooth-muscle antibodies; actin is a ubiquitous contractile protein that can be found in non–muscle cells.[11] Further studies showed that tubular smooth-muscle antibody (SMA-T) and glomerular smooth-muscle antibody (SMA-G) immunofluorescence staining patterns, which predominantly react with filamentous actin (F-actin), were the main antigenic moiety of smooth-muscle antibodies.[12, 13, 14] This was further shown to be present predominantly in a group of patients with chronic active hepatitis later classified as autoimmune hepatitis type 1 (AIH-1).[13, 14, 15]

Immunologic detection

The earliest experiments for detection of smooth-muscle antibodies involved indirect immunofluorescence (IIF).[6, 9] At present, IIF is still the standard method used to detect anti–smooth-muscle antibodies (ASMAs). This technique involves subjecting thin specimens of rodent liver, stomach, or kidney to a patient’s serum. A 1:20 or 1:40 dilution of patient’s serum is used for initial screening. If present in the patient’s serum, antibodies attach to smooth-muscle antigens on the rodent tissue specimens. These primary antibodies are then visualized by tagging them with a fluorescein conjugated anti-immunoglobulin antibody, which serves as the secondary antibody. The tissues are then analyzed with a fluorescence microscope and reported as positive if fluorescent immunostaining is detected. The patient’s serum is then titrated with subsequent dilutions until immunofluorescence is no longer detected.

Indications

ASMA titers can be tested in the evaluation of patients with liver disease suspected to have an underlying autoimmune etiology. The clinical presentation of such patients, however, varies widely and can be generally subdivided into the following:

  • Asymptomatic patients with transaminitis
  • Acute hepatitis
  • Fulminant hepatic failure
  • Chronic active hepatitis
  • Established cirrhosis
  • Overlap syndromes

Owing to the heterogeneity of clinical manifestations, including the possibility of overlap syndromes, ASMA testing can be included as a part of a panel of tests to determine the etiology of liver dysfunction.

Contraindications

No specific contraindications exist for testing ASMA.

Considerations

In investigation of liver dysfunction that may be due to AIH-1, ASMA testing should be performed in conjunction with other ancillary tests under the appropriate clinical scenario. This is especially significant when using scoring systems to determine the likelihood of underlying AIH-1. Some of these tests include immunoglobulin levels, antinuclear antibody, anti–liver kidney microsomal antibody (anti-LKM), and liver cytosol antibody type 1 (anti-LC1), to name a few. In addition, tests to exclude other etiologies also must be performed.

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Contributor Information and Disclosures
Author

Joshua Sloan, DO Resident Physician, Department of Internal Medicine, Einstein Medical Center

Joshua Sloan, DO is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Gentry George T King, MD Chief Resident, Department of Internal Medicine, Albert Einstein Medical Center

Gentry George T King, MD is a member of the following medical societies: Pennsylvania Medical Society, American Society of Clinical Oncology, Philippine Medical Association

Disclosure: Nothing to disclose.

Eyob Feyssa, MD, MPH, FACP Interim Director, Division of Hepatology, Center for Liver Disease and Transplantation, Einstein Healthcare Network, Philadelphia

Eyob Feyssa, MD, MPH, FACP is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, American Gastroenterological Association

Disclosure: Nothing to disclose.

Chief Editor

Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital

Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology

Disclosure: Nothing to disclose.

Acknowledgements

Judy Lin, MD

Disclosure: Nothing to disclose.

References
  1. Alvarez F, Berg PA, Bianchi FB, et al. International Autoimmune Hepatitis Group Report: review of criteria for diagnosis of autoimmune hepatitis. J Hepatol. 1999 Nov. 31(5):929-38. [Medline].

  2. Czaja AJ. Performance parameters of the diagnostic scoring systems for autoimmune hepatitis. Hepatology. 2008 Nov. 48(5):1540-8. [Medline].

  3. Krawitt EL. Autoimmune hepatitis. N Engl J Med. 2006 Jan 5. 354(1):54-66. [Medline].

  4. Cassani F, Cataleta M, Valentini P, et al. Serum autoantibodies in chronic hepatitis C: comparison with autoimmune hepatitis and impact on the disease profile. Hepatology. 1997 Sep. 26(3):561-6. [Medline].

  5. Czaja AJ, Carpenter HA, Santrach PJ, Moore SB. Immunologic features and HLA associations in chronic viral hepatitis. Gastroenterology. 1995 Jan. 108(1):157-64. [Medline].

  6. Johnson GD, Holborow EJ, Glynn LE. Antibody to smooth muscle in patients with liver disease. Lancet. 1965 Oct 30. 2(7418):878-9. [Medline].

  7. Mackay IR. Lupoid hepatitis and primary biliary cirrhosis: autoimmune diseases of the liver. Bull Rheum Dis. 1968. 18:487.

  8. Husby G, Pierce PE, Williams RC Jr. Smooth muscle antibody in heroin addicts. Ann Intern Med. 1975 Dec. 83(6):801-5. [Medline].

  9. Whittingham S, Irwin J, Mackay IR, Smalley M. Smooth muscle autoantibody in "autoimmune" hepatitis. Gastroenterology. 1966 Oct. 51(4):499-505. [Medline].

  10. Gabbiani G, Ryan GB, Lamelin JP, Vassalli P, Majno G, Bouvier CA. Human smooth muscle autoantibody. Its identification as antiactin antibody and a study of its binding to "nonmuscular" cells. Am J Pathol. 1973 Sep. 72(3):473-88. [Medline].

  11. Pollard TD, Weihing RR. Actin and myosin and cell movement. CRC Crit Rev Biochem. 1974 Jan. 2(1):1-65. [Medline].

  12. Lidman K, Biberfeld G, Fagraeus A, Norberg R, Torstensson R, Utter G. Anti-actin specificity of human smooth muscle antibodies in chronic active hepatitis. Clin Exp Immunol. 1976 May. 24(2):266-72. [Medline].

  13. Bottazzo GF, Florin-Christensen A, Fairfax A, Swana G, Doniach D, Groeschel-Stewart U. Classification of smooth muscle autoantibodies detected by immunofluorescence. J Clin Pathol. 1976 May. 29(5):403-10. [Medline].

  14. Toh BH. Smooth muscle autoantibodies and autoantigens. Clin Exp Immunol. 1979 Dec. 38(3):621-8. [Medline].

  15. Czaja AJ, Cassani F, Cataleta M, Valentini P, Bianchi FB. Frequency and significance of antibodies to actin in type 1 autoimmune hepatitis. Hepatology. 1996 Nov. 24(5):1068-73. [Medline].

 
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